A variety of halogenated hydrocarbons are used by man for such diverse things as anesthetics and insecticides. A proportion of these agents produce liver injury--both acute and chronic. The hepatotoxicity of CCl4 may represent a model system for the study of the mechanisms involved in cell injury and in regeneration following injury. Critical analyses of the processes involved may provide clues for devising better tests to screen for potential toxicity of these new compounds. These studies propose to investigate the mechanism of enzymic dehalogenation and its role in CCl4 and to explore the changes in cellular membranous structures during the development of the injury. More specifically, structural and functional changes in the plasmalemma will be detailed. The hypothesis that plasmalemma alterations are a key to cell death will be tested. In addition, the role of altered translocation in decreased protein synthesis will be sought. A comparison of these changes with halothane-induced injury will also be made.